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Protection against kainate neurotoxicity by ginsenosides: attenuation of convulsive behavior, mitochondrial dysfunction, and oxidative stress.
J Neurosci Res. 2009 Feb 15; 87(3):710-22.JN

Abstract

We previously demonstrated that kainic acid (KA)-mediated mitochondrial oxidative stress contributed to hippocampal degeneration and that ginsenosides attenuated KA-induced neurotoxicity and neuronal degeneration. Here, we examined whether ginsenosides affected KA-induced mitochondrial dysfunction and oxidative stress in the rat hippocampus. Treatment with ginsenosides attenuated KA-induced convulsive behavior dose-dependently. KA treatment increased lipid peroxidation and protein oxidation and decreased the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio to a greater degree in the mitochondrial fraction than in the hippocampal homogenate. KA treatment resulted in decreased Mn-superoxide dismutase expression and diminished the mitochondrial membrane potential. Furthermore, KA treatment increased intramitochondrial Ca(2+) and promoted ultrastructural degeneration in hippocampal mitochondria. Treatment with ginsenosides dose-dependently attenuated convulsive behavior and the KA-induced mitochondrial effects. Protection appeared to be more evident in mitochondria than in tissue homogenates. Collectively, the results suggest that ginsenosides prevent KA-induced neurotoxicity by attenuating mitochondrial oxidative stress and mitochondrial dysfunction.

Authors+Show Affiliations

Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18816793

Citation

Shin, Eun-Joo, et al. "Protection Against Kainate Neurotoxicity By Ginsenosides: Attenuation of Convulsive Behavior, Mitochondrial Dysfunction, and Oxidative Stress." Journal of Neuroscience Research, vol. 87, no. 3, 2009, pp. 710-22.
Shin EJ, Jeong JH, Kim AY, et al. Protection against kainate neurotoxicity by ginsenosides: attenuation of convulsive behavior, mitochondrial dysfunction, and oxidative stress. J Neurosci Res. 2009;87(3):710-22.
Shin, E. J., Jeong, J. H., Kim, A. Y., Koh, Y. H., Nah, S. Y., Kim, W. K., Ko, K. H., Kim, H. J., Wie, M. B., Kwon, Y. S., Yoneda, Y., & Kim, H. C. (2009). Protection against kainate neurotoxicity by ginsenosides: attenuation of convulsive behavior, mitochondrial dysfunction, and oxidative stress. Journal of Neuroscience Research, 87(3), 710-22. https://doi.org/10.1002/jnr.21880
Shin EJ, et al. Protection Against Kainate Neurotoxicity By Ginsenosides: Attenuation of Convulsive Behavior, Mitochondrial Dysfunction, and Oxidative Stress. J Neurosci Res. 2009 Feb 15;87(3):710-22. PubMed PMID: 18816793.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protection against kainate neurotoxicity by ginsenosides: attenuation of convulsive behavior, mitochondrial dysfunction, and oxidative stress. AU - Shin,Eun-Joo, AU - Jeong,Ji Hoon, AU - Kim,A-Young, AU - Koh,Young Ho, AU - Nah,Seung-Yeoul, AU - Kim,Won-Ki, AU - Ko,Kwang Ho, AU - Kim,Hyun Ji, AU - Wie,Myung-Bok, AU - Kwon,Yong Soo, AU - Yoneda,Yukio, AU - Kim,Hyoung-Chun, PY - 2008/9/26/pubmed PY - 2009/4/1/medline PY - 2008/9/26/entrez SP - 710 EP - 22 JF - Journal of neuroscience research JO - J Neurosci Res VL - 87 IS - 3 N2 - We previously demonstrated that kainic acid (KA)-mediated mitochondrial oxidative stress contributed to hippocampal degeneration and that ginsenosides attenuated KA-induced neurotoxicity and neuronal degeneration. Here, we examined whether ginsenosides affected KA-induced mitochondrial dysfunction and oxidative stress in the rat hippocampus. Treatment with ginsenosides attenuated KA-induced convulsive behavior dose-dependently. KA treatment increased lipid peroxidation and protein oxidation and decreased the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio to a greater degree in the mitochondrial fraction than in the hippocampal homogenate. KA treatment resulted in decreased Mn-superoxide dismutase expression and diminished the mitochondrial membrane potential. Furthermore, KA treatment increased intramitochondrial Ca(2+) and promoted ultrastructural degeneration in hippocampal mitochondria. Treatment with ginsenosides dose-dependently attenuated convulsive behavior and the KA-induced mitochondrial effects. Protection appeared to be more evident in mitochondria than in tissue homogenates. Collectively, the results suggest that ginsenosides prevent KA-induced neurotoxicity by attenuating mitochondrial oxidative stress and mitochondrial dysfunction. SN - 1097-4547 UR - https://www.unboundmedicine.com/medline/citation/18816793/Protection_against_kainate_neurotoxicity_by_ginsenosides:_attenuation_of_convulsive_behavior_mitochondrial_dysfunction_and_oxidative_stress_ L2 - https://doi.org/10.1002/jnr.21880 DB - PRIME DP - Unbound Medicine ER -